This may be contradictory since the release of NGAL occurs early in granulocyte differentiation [7], and given the high turnover and the short half-life of these cells in endotoxemia [32] as well as the short half-life of NGAL [33], one would have expected that the timing of hydrocortisone should not have impacted on neutrophil activation in these experiments. The gene discussed is LCN2; the disease is serum lipopolysaccharide activity.